Hand and foot dermatitis simply means inflammation of the skin of the hands and/or feet. This nonspecific term is used for several more specific disorders (Table 253-2). The most common causes are contact dermatitis (allergic and irritant), dyshidrosis, and atopic dermatitis. Most contact dermatitis is caused by irritants as opposed to allergens. Atopic dermatitis affects children, usually before 5 years of age, and 2% to 3% of adults.16
TABLE 253-2Differential Diagnosis of Hand and Foot Dermatitis ||Download (.pdf) TABLE 253-2 Differential Diagnosis of Hand and Foot Dermatitis
Allergic contact dermatitis (poison ivy, poison oak, etc.)
Irritant contact dermatitis (soaps, detergents, shoe/glove leather, etc.)
Dermatophytosis (see Table 253-4)
Pityriasis rubra pilaris
Autoimmune bullous disease
Common irritants include soaps, detergents, friction, frequent hand washing, and cold, dry air, resulting in erythema, scaling, and fissuring. Strong irritants like an acid or alkali cause immediate burning, followed by erythema, vesiculation, and bullae formation.
Common allergens include poison ivy/poison oak, nickel, chromate, rubber components of gloves and shoes, dyes in leather and socks, and dichromates used in tanning leather. In acute allergic contact dermatitis, erythema with papules, vesicles, and/or bullae is present. Pruritus is intense, and excoriations are present. Distribution is the most helpful clue to aid in diagnosis. When the hands or feet are involved in allergic contact dermatitis, the eruption tends to be present on the dorsal surfaces, sparing the palms, soles, and web spaces. The thick stratum corneum of the palms and soles prevents penetration of potential allergens. Distribution with linear streaks suggests a plant allergy such as rhus (poison ivy or oak) hypersensitivity (Figure 253-6). Sharp demarcation of footwear indicates a reaction to a component of the patient's shoes.
Allergic contact dermatitis secondary to poison ivy. [Photo contributed by University of North Carolina Department of Dermatology.]
Dyshidrosis initially begins as very small, deep-seated, pruritic vesicles on the lateral aspects and the volar surfaces of the palms and soles (Figure 253-7). The dorsal surface of the distal phalanges may also become involved. There is no erythema. Over time, the vesicles may form pustules or desquamate to leave small collarettes of scales. In chronic cases, erythema and scales become more prominent and may be difficult to distinguish from other forms of hand and foot dermatitis.
Dyshidrosis. Clear, tapioca-like lesions with secondary encrustation. [Photo contributed by University of North Carolina Department of Dermatology.]
Atopic dermatitis is part of the "atopic triad" consisting of dermatitis, asthma, and allergic rhinitis.17 Atopic dermatitis of the hands and feet often presents as erythematous, pruritic, scaly patches with prominent involvement of the dorsal surfaces as well as the palms and soles. Chronic atopic dermatitis will also have hyperpigmentation and lichenification and fissuring. Often, other areas of the body are involved. Common areas of involvement include the antecubital and popliteal fossae, posterior neck, and wrists and ankles (Figure 253-8).
Atopic dermatitis with lichenification. [Photo contributed by University of North Carolina Department of Dermatology.]
The diagnosis is clinical. Differentiating contact dermatitis (allergic and irritant) from dyshidrosis and atopic dermatitis can be extremely difficult. More than one disorder may be present at a time, such as atopic dermatitis complicated by irritant dermatitis. Always consider a fungal infection (see later section "Tinea Pedis and Tinea Manuum"), and a potassium hydroxide preparation can exclude this possibility. A biopsy cannot differentiate between the different types of dermatitis. See Table 253-3 for definitions of terms in superficial cutaneous fungal infections and Table 253-4 for causes of superficial cutaneous fungal infections. Dermatologic consultation is often necessary for specific diagnosis.
TABLE 253-3Definitions of Terms for Superficial Cutaneous Fungal Infections ||Download (.pdf) TABLE 253-3 Definitions of Terms for Superficial Cutaneous Fungal Infections
Dermatophytes: a group of fungi that infect nonviable keratinized cutaneous structures such as stratum corneum, nails, and hair. They most commonly include Trichophyton species, Microsporum species, and Epidermophyton species.
Dermatophytosis: an infection caused by dermatophytes
Tinea: a term used for specific clinical manifestations of dermatophyte or dermatophyte-like infections, with the addition of a term that usually indicates the anatomic area affected (tinea pedis, tinea manuum, etc.)
Malassezia species: a yeast causing tinea versicolor or pityriasis versicolor
TABLE 253-4Causes of Superficial Cutaneous Fungal Infections ||Download (.pdf) TABLE 253-4 Causes of Superficial Cutaneous Fungal Infections
Trichophyton species (cause most superficial cutaneous fungal infections)
Treatment is the removal of offending agents. Antihistamine, anesthetic, antibiotic, and anti-itch creams should be stopped because they may cause a second allergy. Lubricate with petroleum jelly, or thick ointments with a petroleum base, frequently and liberally.
For acute eruptions with vesiculation, use aluminum acetate, two to three times per day. Mix one aluminum acetate powder packet or tablet with 1 pint of water, and then apply with a towel or gauze to the affected area for 15 to 20 minutes. Use a high-potency topical corticosteroid, such as clobetasol ointment, twice a day, after the compress. Hydroxyzine, 25 to 50 milligrams up to four times a day, can relieve itching.
In severe cases with debilitating eruptions, systemic glucocorticoids are indicated. For poison ivy or oak, give oral prednisone, 60 milligrams/d, for 2 to 3 weeks. Shorter courses of prednisone can result in relapse.
Treat chronic eruptions with high-potency topical corticosteroids two to three times a day. Ointments are preferred because they help with lubrication. Systemic glucocorticoids should be avoided in chronic cases and atopic dermatitis. Although systemic steroids may provide temporary relief, rebound activity after cessation is common.
Psoriasis vulgaris or plaque-type psoriasis may involve only the palms and soles but often extends to other areas, especially the elbows, knees, scalp, umbilicus, and gluteal cleft (see chapter 251 for more discussion). If pustules are present, the disorder is called pustular psoriasis. Peak ages of onset are between 20 and 30 years old and between 50 and 60 years old.
Psoriasis is an inherited disease in which the principal abnormality is believed to be an abnormal T lymphocyte–driven immune process. These altered T cells are believed to secrete cytokines that shorten the keratinocyte cell cycle and produce arthropathy.
Psoriasis is characterized by discrete plaques of erythema, scales, and fissures on the extremities (Figure 253-9). Extensive disease may extend over the entire palms, soles, and dorsal surfaces of the hands or feet (Figure 253-10). Onycholysis (separation of the nail plate from the nail bed), nail pits, and yellow discoloration of the nails help support the diagnosis of psoriasis (Figure 253-11).
Psoriasis vulgaris. [Photo contributed by University of North Carolina Department of Dermatology.]
Psoriasis vulgaris of the plantar foot. [Photo contributed by University of North Carolina Department of Dermatology.]
Psoriasis nails. [Photo contributed by University of North Carolina Department of Dermatology.]
In pustular psoriasis of the palms and soles, erythema, minimal scale, and numerous sterile pustules are seen. The pustules are in various stages of evolution from small pustules to larger confluent "lakes of pus" to crusts to rings of scale (Figure 253-12). Pustules are most commonly seen bilaterally on the instep of the foot and the thenar and hypothenar eminences of the hands.
Pustular psoriasis. [Photo contributed by University of North Carolina Department of Dermatology.]
Complete examination of the skin focusing on the sites commonly affected by psoriasis, including the elbows, knees, scalp, lower back, gluteal cleft, umbilicus, and nails, may reveal other areas of involvement to aid in diagnosing psoriasis. If no other psoriatic plaques are noted, differentiation from hand and foot dermatitis can be difficult (Table 253-5). A biopsy may be helpful in this instance. A potassium hydroxide examination should be performed to exclude a dermatophyte infection. Bacterial and viral cultures should be obtained when disease is pustular and localized to one area.
TABLE 253-5Differential Diagnosis of Psoriasis ||Download (.pdf) TABLE 253-5 Differential Diagnosis of Psoriasis
Hand and foot dermatitis
Lichen simplex chronicus
Tinea pedis and tinea manuum
Staphylococcus aureus infection
Herpes simplex infection
Initial treatment includes the use of a high- or ultrahigh-potency topical corticosteroid such as fluocinonide, clobetasol propionate, or betamethasone dipropionate ointment. Encourage liberal use of white petrolatum-based topical emollients. Do not prescribe systemic steroids because of the risk of rebound or induction of pustular psoriasis. The disease is chronic and slow to respond to treatment. Arrange follow-up with a dermatologist.
Erythema nodosum is an inflammatory eruption of the subcutaneous fat. It has many possible causes (Table 253-6) and is idiopathic in nearly half of cases. All age groups can be affected.
TABLE 253-6Causes of Erythema Nodosum ||Download (.pdf) TABLE 253-6 Causes of Erythema Nodosum
|Infectious ||Pharmacologic |
| Fungal || Sulfonamides |
| Blastomycosis || Oral contraceptive pills |
| Coccidioidomycosis || Penicillin |
| Histoplasmosis || Bromides |
| Dermatophyte || Vaccines |
|Bacterial ||Sarcoidosis |
| Streptococcal infections ||Inflammatory bowel disease |
|Campylobacter ||Pregnancy |
|Yersiniaspecies ||Behçet's syndrome |
| Tuberculosis ||Leukemia and lymphoma |
| Leprosy ||Idiopathic |
|Parasitic || |
| Leishmaniasis || |
| Toxoplasmosis || |
|Viral || |
| Herpes simplex || |
| Infectious mononucleosis || |
Tender, warm, ill-defined erythematous nodules characterize erythema nodosum (Figure 253-13). Nodules are most commonly seen on the pretibial area of the lower extremities, although the extensor aspects of the arms and torso can occasionally be involved. Ulceration is not a feature and suggests another diagnosis. Nodules can persist for weeks.
Erythema nodosum—painful palpable erythematous nodules. [Photo contributed by University of North Carolina Department of Dermatology.]
The diagnosis is clinical and should include evaluation for possible causes (Table 253-6). If the diagnosis is unclear (Table 253-7), refer for a biopsy.
TABLE 253-7Differential Diagnosis of Erythema Nodosum ||Download (.pdf) TABLE 253-7 Differential Diagnosis of Erythema Nodosum
Erythema induratum (nodular vasculitis)
Connective tissue panniculitis
Malignant subcutaneous infiltrates
Cytophagic histiocytic panniculitis
Infection (fungal, bacterial, or mycobacterial)
Treatment is symptomatic, with leg elevation and nonsteroidal anti-inflammatory drugs. Treat the underlying cause. Refer refractory cases to a dermatologist.
LICHEN SIMPLEX CHRONICUS, CORNS, AND CALLUSES
Lichen simplex chronicus, corns, and calluses are all thickenings of the upper layer of the skin (stratum corneum) in response to chronic friction and scratching. Most commonly, ankles, lower extremities, neck, scrotum, and vulva are involved. When friction occurs in the absence of pruritus and is distributed over a large area, a callus is formed. When the same frictional forces occur over a localized area of the foot, a corn is formed. Calluses and corns are most commonly located on the feet.
Lichen simplex chronicus presents as one or several intensely pruritic, well-demarcated plaques, with lichenification because of chronic scratching and rubbing (Figure 253-14). Erythema, hyperpigmentation, and excoriations are also present. Scale is minimal. The ankles, shins, dorsal feet, and hands may be affected.
Lichen simplex chronicus. [Photo contributed by University of North Carolina Department of Dermatology.]
Calluses and corns present as thickened plaques at areas of repetitive trauma. Corns form firm, dome-shaped papules with translucent central cores on the dorsal, lateral, and interdigital toes (Figure 253-15).
Corn. Painful, hyperkeratotic lesion. [Photo contributed by University of North Carolina Department of Dermatology.]
Diagnosis is clinical (Table 253-8). A potassium hydroxide examination can be helpful to rule out a dermatophyte infection. If the diagnosis is uncertain, refer for a skin biopsy. Paring of warts reveals punctuate thrombosed capillaries, which are not found in calluses or corns.
TABLE 253-8Differential Diagnosis of Lichen Simplex Chronicus, Corns, and Calluses ||Download (.pdf) TABLE 253-8 Differential Diagnosis of Lichen Simplex Chronicus, Corns, and Calluses
Lichen simplex chronicus
Squamous cell carcinoma
Corns and calluses
Squamous cell carcinoma
Punctuate palmoplantar keratoses
Poroma (benign hair follicle tumor)
For lichen simplex chronicus, interrupting the scratch–itch cycle is the most important aspect of treatment. High-potency topical corticosteroids such as fluocinonide or clobetasol ointment should be applied to the plaque two to three times a day. Oral antihistamines help for pruritus.
Paring and keratolytics, such as salicylic acid, are first-line treatments for corns and calluses, as well as proper footwear and medical management.18 For further treatment, refer to a podiatrist or dermatologist.
Dermatitis herpetiformis is a cutaneous manifestation of gluten sensitivity. It is most common in individuals of northern European descent.19 Often, there is familial involvement, and there is almost universal association with HLA-DQ2 or HLA-DQ8, located on chromosome 6, with close relatives being affected by either dermatitis herpetiformis or celiac disease.20
Granular deposits of immunoglobulin A are found at the dermal–epidermal junction of all patients with dermatitis herpetiformis. These deposits are believed to attract neutrophils, which induce vesicle formation. The presence of immunoglobulin A antibodies to tissue transglutaminase is also highly sensitive and specific for the disorder.21
Extremely pruritic vesicles, papules, or urticarial plaques are symmetrically distributed on extensor surfaces of the extremities, back, and buttocks (Figure 253-16). Chronic scratching may result in excoriations and lichenification in these locations. Approximately 20% of patients will have clinical evidence of malabsorption.22
Dermatitis herpetiformis. Papules and vesicles are grouped together, not in a dermatomal distribution, and are symmetrically distributed on extensor areas of elbows and knees. [Reproduced with permission from Wolff KL, Johnson R, Suurmond R: Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology, 5th ed. © 2005, McGraw-Hill, New York.]
The diagnosis is supported by clinical, biopsy, and laboratory findings (Table 253-9). Diagnosis and treatment require dermatology referral.
TABLE 253-9Differential Diagnosis of Dermatitis Herpetiformis ||Download (.pdf) TABLE 253-9 Differential Diagnosis of Dermatitis Herpetiformis
Bullous lupus erythematosus
Linear immunoglobulin A bullous dermatosis
Atopic dermatitis (eczema)
Treatment for dermatitis herpetiformis includes oral dapsone and a gluten-free diet. Oral dapsone relieves pruritus within 72 hours of beginning therapy. Systemic steroids are ineffective.